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2014 Fiscal Year Final Research Report

Role of Rho family in cAMP-dependent exocrine secretion

Research Project

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Project/Area Number 24580433
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Basic veterinary science/Basic zootechnical science
Research InstitutionNihon University

Principal Investigator

SUGIYA Hiroshi  日本大学, 生物資源科学部, 教授 (20050114)

Co-Investigator(Renkei-kenkyūsha) NARITA Takanori  日本大学, 生物資源科学部, 専任講師 (70453884)
OKABAYASHI Ken  日本大学, 生物資源科学部, 専任講師 (20409072)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords生理・細胞機能 / 耳下腺 / 開口分泌 / cAMP / Rho / Rhoキナーゼ / アクチン
Outline of Final Research Achievements

In rat parotid acinar cells, stimulation of β-adrenergic receptors provokes an increase in intracellular cAMP level, resulting in amylase release. We studied involvement of Rho family, a member of Ras superfamily proteins, in the amylase release. A protein band ADP-ribosylated by Clostridium botulinum C3 (C3), an inhibitor of the function via ADP-ribosylation of Rho, was detected in the cells. The same protein band was cross-reacted with anti-RhoA antibody. RhoA was activated by the β-agonist isoproterenol (IPR). C3 blocked the cAMP-induced amylase release in permeabilized cells. The IPR-induced RhoA activation was inhibited by a PKA inhibitor. The Rho kinase inhibitor Y-27632 partially inhibited the IPR-induced and dibutyryl cAMP-induced amylase release. In the cells treated with Y-27632, IPR-induced distribution of cortical F-actin was disturbed. These results suggest that RhoA/ROCK signaling is involved in cAMP-dependent amylase release in rat parotid acinar cells.

Free Research Field

農学

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Published: 2016-06-03  

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